Chromosomal and extrachromosomal instability of the cyclin D2 gene is induced by Myc overexpression.

We examined the expression of cyclins D1, D2, D3, and E in mouse B-lymphocytic tumors. Cyclin D2 mRNA was consistently elevated in plasmacytomas, which characteristically contain Myc-activating chromosome translocations and constitutive c-Myc mRNA and protein expression. We examined the nature of cyclin D2 overexpression in plasmacytomas and other tumors.

Direct induction of cyclin D2 by Myc contributes to cell cycle progression and sequestration of p27.

Ectopic expression of Myc induces Cdk2 kinase activity in quiescent cells and antagonizes association of p27(kip1) with Cdk2. The target gene(s) by which Myc mediates this effect is largely unknown. We now show that p27 is rapidly and transiently sequestered by cyclin D2-Cdk4 complexes upon activation of Myc and that cyclin D2 is a direct target gene of Myc.

G1 cyclins and control of the cell division cycle in normal and transformed cells.

The G1 cyclins are clearly important factors that control progression through the eukaryotic cell cycle. The expression and activity of these factors are regulated at many different levels and in response to a large number of signals. Such complicated, multilevel controls on expression and activation of cyclin/cdk complexes permit exquisite and necessary coordination of the stages of the cell cycle.

c-Myc overexpression associated DHFR gene amplification in hamster, rat, mouse and human cell lines.

We have analysed relative DHFR gene copy numbers in nine cell lines of various cell type and species origins. The cells studied expressed either low, low and inducible or constitutively elevated levels of c-Myc protein. DHFR gene amplification was observed only when c-Myc protein levels were upregulated.